ArticleInternational journal of molecular sciences2022
CYP1B1 Augments the Mesenchymal, Claudin-Low, and Chemoresistant Phenotypes of Triple-Negative Breast Cancer Cells.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Pharmacogenetic CYP2B6 variants affect steroid hormone metabolism in human breast cancer cells.British journal of clinical pharmacology · 2026Article
- The significance of immunogenic cell death related prognostic gene markers in colorectal cancer prognosis and antitumor immunity.Scientific reports · 2026Article
- Pericyte-derived cancer-associated fibroblasts correlate with poor survival and are enriched after chemoradiotherapy in glioblastoma.PloS one · 2026Article
- Integrative multi-omics reveals common and distinct pathogenic mechanisms and preoperative diagnostic signatures in breast fibroepithelial lesions.Breast cancer research : BCR · 2025Article
- Protein-Level Analysis of Differential Response to Chemotherapy in Triple-Negative Breast Cancer Identifies CYP1B1 as a Biomarker for Chemotherapy Resistance.Cancer research communications · 2025Article
- ADME gene-driven prognostic model for bladder cancer: a breakthrough in predicting survival and personalized treatment.Hereditas · 2025Article
- The mRNA MOXD1: Link to oxidative stress and prognostic significance in gastric cancer.Open medicine (Warsaw, Poland) · 2025Article
- Molecular Research and Treatment of Breast Cancer 2.0.International journal of molecular sciences · 2024Article
- Adipocyte-derived kynurenine stimulates malignant transformation of mammary epithelial cells through the aryl hydrocarbon receptor.Biochemical pharmacology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cytochrome P4501B1 (CYP1B1) is elevated in breast cancer. Studies indicate a relationship between CYP1B1 and aggressive cancer phenotypes. Here, we report on in vitro studies in triple-negative breast cancer cell lines, where knockdown (KD) of CYP1B1 was used to determine the influence of its expression on invasive cell phenotypes. CYP1B1 KD in MDA-MB-231 cells resulted in the loss of mesenchymal morphology, altered expression of epithelial-mesenchymal genes, and increased claudin (CLDN) RNA and protein. CYP1B1 KD cells had increased cell-to-cell contact and paracellular barrier function, a reduced rate of cell proliferation, abrogation of migratory and invasive activity, and diminished spheroid formation. Analysis of clinical breast cancer tumor samples revealed an association between tumors exhibiting higher CYP1B1 RNA levels and diminished overall and disease-free survival. Tumor expression of CYP1B1 was inversely associated with CLDN7 expression, and CYP1B1
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.